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Updated: Sep 18, 2025

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Resveratrol Mitigates Inflammation by Modulating Tumor Necrosis Factor-Alpha Receptors (TNFRs) in a

Médea Veszelka1,2, József Hegyközi2,3, Nikoletta Almási1,2

  • 1Department of Physiology, Anatomy, and Neuroscience, Faculty of Science and Informatics, University of Szeged, 6726 Szeged, Hungary.

International Journal of Molecular Sciences
|June 26, 2025
PubMed

Insights

Resveratrol (RES) shows promise for inflammatory bowel disease (IBD). A 10 mg/kg dose in rats significantly reduced colitis symptoms and inflammation by modulating tumor necrosis factor-alpha (TNF-α) signaling.

Area of Science:

  • Gastroenterology
  • Pharmacology
  • Molecular Biology

Background:

  • Inflammatory bowel disease (IBD) is a chronic condition requiring novel treatments.
  • Resveratrol (RES), a natural polyphenol, possesses antioxidant and anti-inflammatory properties.
  • RES is being explored for its therapeutic potential in IBD management.

Purpose of the Study:

  • To investigate the efficacy of resveratrol (RES) as a potential treatment for TNBS-induced colitis in rats.
  • To evaluate the impact of RES on colonic ulceration, pro-inflammatory cytokines, and TNF receptor signaling.

Main Methods:

  • Male Wistar-Hannover rats were administered oral RES (5, 10, or 20 mg/kg/day) for 28 days.
  • Colitis was induced via intracolonic instillation of 2,4,6-trinitrobenzene sulphonic acid (TNBS).
  • Histological, planimetric, and immunohistochemical analyses were performed to assess treatment effects.

Main Results:

  • The 10 mg/kg RES dose significantly reduced colonic ulceration and tumor necrosis factor-alpha (TNF-α) expression.
  • RES treatment attenuated the intensity of TNF-α receptors (TNFR1 and TNFR2).
  • Elevated lipocalin-2 (Lcn-2) levels in TNBS-induced colitis were observed.

Conclusions:

  • Resveratrol (RES) demonstrates protective effects in a rat model of colitis.
  • RES may exert its benefits partly by modulating TNF receptor signaling pathways.
  • RES shows potential as an adjunctive or standalone therapy for inflammatory bowel disease.
Keywords:
IBDTNBS-induced colitisTNF-alphaTNFR-α receptorcolon inflammationoxidative stresspro-inflammatory cytokineresveratrol

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